The fact that the FRβ is most prominently expressed on the Mono‐AMs and that this macrophage subpopulation contributes disproportionately to the development of lung fibrosis (Misharin et al, 2017) supports the contention that delivery of anti‐fibrotic drugs using an FRβ targeting strategy should treat fibrosis without damaging healthy tissues. The gene discussed is FOLR2; the disease is pulmonary fibrosis.